Abstract
It is becoming increasingly evident that Helicobacter pylori have been normal inhabitants of the human stomach since the earliest times (1) and that, over the course of the twentieth century, H. pylori has been disappearing (2). Because large groups of people can be identified who either do or do not carry the organism, we now can assess the consequences of its presence (and absence). Such studies have shown that the presence of H. pylori is associated with the development of all of the important precursor lesions for adenocarcinoma of the stomach, including chronic gastritis, atrophic gastritis, and intestinal metaplasia and that, in consequence, it is the major risk factor for non-cardia gastric cancers (3,4).

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